scholarly journals Pancreatic damage in COVID‐19: Why? How?

Author(s):  
Ferhat Bacaksız ◽  
Berat Ebik ◽  
Nazım Ekin ◽  
Jihat Kılıc
Keyword(s):  
Author(s):  
Ranjit Unnikrishnan ◽  
Anoop Misra

AbstractThe advent and rapid spread of the coronavirus disease-2019 (COVID19) pandemic across the world has focused attention on the relationship of commonly occurring comorbidities such as diabetes on the course and outcomes of this infection. While diabetes does not seem to be associated with an increased risk of COVID19 infection per se, it has been clearly demonstrated that the presence of hyperglycemia of any degree predisposes to worse outcomes, such as more severe respiratory involvement, ICU admissions, need for mechanical ventilation and mortality. Further, COVID19 infection has been associated with the development of new-onset hyperglycemia and diabetes, and worsening of glycemic control in pre-existing diabetes, due to direct pancreatic damage by the virus, body’s stress response to infection (including cytokine storm) and use of diabetogenic drugs such as corticosteroids in the treatment of severe COVID19. In addition, public health measures taken to flatten the pandemic curve (such as lockdowns) can also adversely impact persons with diabetes by limiting their access to clinical care, healthy diet, and opportunities to exercise. Most antidiabetic medications can continue to be used in patients with mild COVID19 but switching over to insulin is preferred in severe disease.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ranjit Unnikrishnan ◽  
Anoop Misra

AbstractThe advent and rapid spread of the coronavirus disease-2019 (COVID19) pandemic across the world has focused attention on the relationship of commonly occurring comorbidities such as diabetes on the course and outcomes of this infection. While diabetes does not seem to be associated with an increased risk of COVID19 infection per se, it has been clearly demonstrated that the presence of hyperglycemia of any degree predisposes to worse outcomes, such as more severe respiratory involvement, ICU admissions, need for mechanical ventilation and mortality. Further, COVID19 infection has been associated with the development of new-onset hyperglycemia and diabetes, and worsening of glycemic control in pre-existing diabetes, due to direct pancreatic damage by the virus, body’s stress response to infection (including cytokine storm) and use of diabetogenic drugs such as corticosteroids in the treatment of severe COVID19. In addition, public health measures taken to flatten the pandemic curve (such as lockdowns) can also adversely impact persons with diabetes by limiting their access to clinical care, healthy diet, and opportunities to exercise. Most antidiabetic medications can continue to be used in patients with mild COVID19 but switching over to insulin is preferred in severe disease.


Digestion ◽  
2007 ◽  
Vol 75 (2-3) ◽  
pp. 156-163 ◽  
Author(s):  
Angelo Andriulli ◽  
Rosario Forlano ◽  
Grazia Napolitano ◽  
Pasquale Conoscitore ◽  
Nazario Caruso ◽  
...  

2010 ◽  
Vol 222 (4) ◽  
pp. 265-273 ◽  
Author(s):  
Yan Yan Fu ◽  
Kyung Ja Kang ◽  
Jung Myung Ahn ◽  
Hae-Ryoung Kim ◽  
Ki Young Na ◽  
...  

2020 ◽  
Author(s):  
Tamara Madácsy ◽  
Árpad Varga ◽  
Noémi Papp ◽  
Barnabás Deák ◽  
Bálint Tél ◽  
...  

ABSTRACTExocrine pancreatic damage is a common complication of cystic fibrosis (CF), which can significantly debilitate the quality of life and life expectancy of CF patients. The cystic fibrosis transmembrane conductance regulator (CFTR) has a major role in pancreatic ductal ion secretion, however, it presumably has an influence on intracellular signaling as well. Here we describe in multiple model systems, including iPSC-derived human pancreatic organoids from CF patients, that the activity of PMCA4 is impaired by the decreased expression of CFTR in ductal cells. The regulation of PMCA4, which colocalizes and physically interacts with CFTR on the apical membrane of the ductal cells, is dependent on the calmodulin binding ability of CFTR. Moreover, CFTR seems to be involved in the process of the apical recruitment of calmodulin, which enhances its role in calcium signaling and homeostasis. Sustained intracellular Ca2+ elevation in CFTR KO cells undermined the mitochondrial function and increased apoptosis. Based on these, the prevention of sustained intracellular Ca2+ overload may improve the exocrine pancreatic function and may have a potential therapeutic aspect in CF.


2010 ◽  
Vol 57 (4) ◽  
Author(s):  
Jaroslaw Walkowiak ◽  
Irena Jankowska ◽  
Aleksandra Lisowska ◽  
Maciej Biczysko ◽  
Aldona Wierzbicka ◽  
...  

High prevalence of elevated serum pancreatic enzymes in children with cholestasis with normal fecal elastase-1 concentrations has been documented. However, this state is related predominantly to biliary atresia. Therefore, we aimed to assess pancreatic damage by measuring serum pancreatic enzymes in patients with progressive familial intrahepatic cholestasis type 2 (PFIC type 2). Twenty PFIC type 2 patients with normal serum bilirubin and bile acid concentrations were included in the study. Thirty pancreatic insufficient cystic fibrosis (PI-CF) patients, thirty patients with acute pancreatitis (AP) and thirty healthy subjects (HS) served for the purpose of comparison. In all subjects, serum lipase and elastase-1 levels were measured. In all but one PFIC type 2 patients and all HS normal lipase activities were found. Serum elastase-1 concentrations were normal in all PFIC type 2 patients and HS. The enzyme levels were very similar in both groups studied. Lipase activities in PFIC type 2 patients were significantly higher than in PI-CF patients (p < 0.00001) and lower than in patients with AP (p < 0.00001). Serum elastase-1 levels in PFIC type 2 patients were significantly lower than in patients with AP (p < 0.00001) and not different from those in PI-CF patients. In conclusion. serum pancreatic enzymes in patients with PFIC type 2 are normal. No pancreatic damage in these patients could be detected.


Amino Acids ◽  
2009 ◽  
Vol 38 (2) ◽  
pp. 575-581 ◽  
Author(s):  
Mervi T. Hyvönen ◽  
Riitta Sinervirta ◽  
Nikolay Grigorenko ◽  
Alex R. Khomutov ◽  
Jouko Vepsäläinen ◽  
...  

1977 ◽  
Vol 47 (6) ◽  
pp. 917-922 ◽  
Author(s):  
Michael E. Carey ◽  
Francis C. Nance ◽  
Homer D. Kirgis ◽  
Harold F. Young ◽  
Lloyd C. Megison ◽  
...  

✓ Six cases of pancreatitis following spinal cord injury are presented. No single, etiologically accepted mechanism already postulated to cause pancreatitis can account for all the cases reported. The authors hypothesize that spinal cord disruption may produce pancreatitis by sympathetic-parasympathetic nervous system imbalance resulting in over-stimulation of the sphincter of Oddi. This may lead to stasis of secretions with absorption of amylase into the systemic circulation, and structural pancreatic damage. Pancreatitis in those with cord injuries is easily overlooked because abdominal pain is usually absent and fever is usually attributed to more frequently occurring pulmonary or urinary tract infections. Recognition of this complication is important in order to decrease the morbidity and mortality that follows spinal cord damage.


1970 ◽  
pp. 249-251
Author(s):  
Raúl Yazigi J. ◽  
Bernardita Lazo
Keyword(s):  

2020 ◽  
Vol 96 (1) ◽  
pp. 28-40 ◽  
Author(s):  
Ahmet Uyar ◽  
Turan Yaman ◽  
Omer Faruk Keles ◽  
Elif Ebru Alkan ◽  
Abdulbaki Demir ◽  
...  

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